Yvonne Myal
Professor
Rady Faculty of Health Sciences
Canada
Biography
B.Sc. Hons (Biology), Univ. of Winnipeg, 1981 M.Sc. (Physiology), Univ. of Manitoba, 1983 Ph.D. (Physiology), Univ. of Manitoba, 1989 Postdoctoral Fellow, (Physiology), Univ of Manitoba, 1989-1992 Research Associate, (Physiology), Univ. Of Manitoba, 1992-1996 Assistant Professor (Physiology), Univ. of Manitoba, 1997-2003 Associate Professor (Physiology), University of Manitoba, 2003- 2010 Professor (Physiology), University of Manitoba, 2010- present Director/Lab Scientist, Molecular Diagnostic Pathology Laboratory Health Sciences Centre, 1997- present
Research Interest
My overall research program is aimed at identifying breast/breast cancer specific biomarkers and understanding the biological role of these markers in tumorigenesis and breast cancer progression. We are currently focusing our efforts on two highly breast specific genes in my laboratory. One, the human small breast epithelial mucin (hSBEM) is a novel human gene recently identified for the first time by us (Myal et al., 2002). We are developing ways of measuring hSBEM in the serum of breast cancer patients and healthy controls. hSBEM has the potential to be a biomarker for the early detection of breast cancer. The other gene we are studying is the human prolactin inducible protein/gross cystic disease fluid protein (hPIP/GCDFP-15) gene. The hPIP/GCDFP-15 is an established biomarker for abnormal breast functions but its role in the progression of breast cancer and in normal breast development is not known. At present we are trying to elucidate the role of hPIP/GCDFP-15 in normal development and mammary gland transformation, using gene knockout strategies. We are also examining the alteration of gene expression in the involuting mammary gland in order to identify novel genes that may be key players in cell proliferation and cell death. A better understanding of this normal physiological process has implications for breast cancer management, as such knowledge will allow for the development of better therapeutic strategies that can directly influence cell proliferation/cell death pathways.